TET2 mutations are associated with hypermethylation at key regulatory enhancers in normal and malignant hematopoiesis
Open accessAbstract
Mutations in the epigenetic modifier TET2 are frequent in myeloid malignancies and clonal hematopoiesis of indeterminate potential (CHIP) and clonal cytopenia of undetermined significance (CCUS). Here, we investigate associations between TET2 mutations and DNA methylation in whole blood in 305 elderly twins, 15 patients with CCUS and 18 healthy controls. We find that TET2 mutations are associated with DNA hypermethylation at enhancer sites in whole blood in CHIP and in both granulocytes and mononuclear cells in CCUS. These hypermethylated sites are associated with leukocyte function and immune response and ETS-related and C/EBP-related transcription factor motifs. While the majority of TET2- associated hypermethylation sites are shared between CHIP and in AML, we find a set of AML-specific hypermethylated loci at active enhancer elements in hematopoietic stem cells. In summary, we show that TET2 mutations is associated with hypermethylated enhancers involved in myeloid differentiation in both CHIP, CCUS and AML patients.
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Hypermethylation in and around PU.1 DNA-binding sites in preleukemic hematopoietic stem and progenitor cells supports that perturbed PU.1-dependent gene regulation may precede AML.
“Moreover, hypermethylation in and around PU.1 DNA-binding sites in preleukemic hematopoietic stem and progenitor cells (28) further supports that perturbed PU.1-dependent gene regulation may precede AML.”
From PU.1-Dependent Enhancer Inhibition Separates <i>Tet2</i> -Deficient Hematopoiesis from Malignant Transformation (2022) · cites this paper as [28]
The Results section on transcription-factor motifs reports hypermethylated enhancer regions enriched for SPI1 (PU.1) motifs in premalignant CHIP and CCUS. However, those analyses used blood-cell samples and monocyte enhancer annotations; they do not establish hypermethylation at measured PU.1-binding sites in preleukemic hematopoietic stem and progenitor cells. The Discussion suggests that hypermethylation in CHIP may be an early event toward malignancy, but the cell type and binding-site specificity in the cited clause are not supported. (LLM, conf=0.86)
Experimental — accuracy not yet measuredSites with aberrant DNA methylation in TET2 or DNMT3A mutant cells are enriched for several key hematopoiesis-regulating transcription factors, including PU.1.
“Sites with aberrant DNA methylation in TET2 or DNMT3A mutant cells are enriched for several key hematopoiesis regulating TF, including PU.1 (28, 45)”
From PU.1-Dependent Enhancer Inhibition Separates <i>Tet2</i> -Deficient Hematopoiesis from Malignant Transformation (2022) · cites this paper as [28]
The Results section (‘TET2-associated hypermethylation co-localizes with specific transcription factor motifs’; page unavailable) reports enrichment of hematopoietic transcription-factor motifs, including SPI1 (PU.1), near TET2-associated hypermethylation in CHIP and CCUS. It does not report the same enrichment for DNMT3A-mutant cells, so the DNMT3A portion is unsupported by this paper. (LLM, conf=0.88)
Experimental — accuracy not yet measuredAltered DNA methylation is prevalent in the elderly, as observed in ARCH, which often precedes AML.
“Altered DNA methylation is prevalent in the elderly, such as observed and well characterized in ARCH (28), which often precedes AML (5).”
From PU.1-Dependent Enhancer Inhibition Separates <i>Tet2</i> -Deficient Hematopoiesis from Malignant Transformation (2022) · cites this paper as [28]
The Introduction and Results describe TET2-associated DNA hypermethylation in elderly people with CHIP, supporting the ARCH example. The source does not establish that altered DNA methylation is prevalent among elderly people generally. The separate claim that ARCH often precedes AML is attached to citation (5), not this source. (LLM, conf=0.85)
Experimental — accuracy not yet measuredTET2-mutant immature and myeloid cells present with hypermethylation of active enhancers and perturbed TF activity.
“Consistently, TET2-mutant immature and myeloid cells present with hypermethylation of active enhancers and perturbed TF activity (28, 32, 53).”
From PU.1-Dependent Enhancer Inhibition Separates <i>Tet2</i> -Deficient Hematopoiesis from Malignant Transformation (2022) · cites this paper as [28]
The Results sections on chromatin states and AML report TET2-associated hypermethylation at monocyte and hematopoietic stem-cell enhancers. The transcription-factor analysis finds enriched binding motifs and suggests a link to transcription-factor recruitment, but does not establish that transcription-factor activity is perturbed. (LLM, conf=0.86)
Experimental — accuracy not yet measured
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“DISCUSSION Altered DNA methylation is prevalent in the elderly, such as observed and well characterized in ARCH (28), which often precedes AML (5).”
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Additional file 5 of Vitamin C boosts DNA demethylation in TET2 germline mutation carriers
Taira, A., Palin, K., Kuosmanen, A., Välimäki, N., Kuittinen, O. M., Kuismin, O., Kaasinen, E., Rajamäki, K., & Aaltonen, L. A. (2024) · Figshare · doi:10.6084/m9.figshare.26561383
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Self-citationAdditional file 4 of Vitamin C boosts DNA demethylation in TET2 germline mutation carriers
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Additional file 2 of Vitamin C boosts DNA demethylation in TET2 germline mutation carriers
Taira, A., Palin, K., Kuosmanen, A., Välimäki, N., Kuittinen, O. M., Kuismin, O., Kaasinen, E., Rajamäki, K., & Aaltonen, L. A. (2024) · Figshare · doi:10.6084/m9.figshare.26561374
Additional file 6 of Vitamin C boosts DNA demethylation in TET2 germline mutation carriers
Taira, A., Palin, K., Kuosmanen, A., Välimäki, N., Kuittinen, O. M., Kuismin, O., Kaasinen, E., Rajamäki, K., & Aaltonen, L. A. (2024) · Figshare · doi:10.6084/m9.figshare.26561386
Additional file 3 of Vitamin C boosts DNA demethylation in TET2 germline mutation carriers
Taira, A., Palin, K., Kuosmanen, A., Välimäki, N., Kuittinen, O. M., Kuismin, O., Kaasinen, E., Rajamäki, K., & Aaltonen, L. A. (2024) · Figshare · doi:10.6084/m9.figshare.26561377
Additional file 1 of Vitamin C boosts DNA demethylation in TET2 germline mutation carriers
Taira, A., Palin, K., Kuosmanen, A., Välimäki, N., Kuittinen, O. M., Kuismin, O., Kaasinen, E., Rajamäki, K., & Aaltonen, L. A. (2024) · Figshare · doi:10.6084/m9.figshare.26561371
- Authors
- Tulstrup, M., Soerensen, M., Hansen, J. W., Gillberg, L., Needhamsen, M., Kaastrup, K., Helin, K., Christensen, K., Weischenfeldt, J., & Grønbæk, K.
- Affiliations
- University of Copenhagen (DK)
- University of Southern Denmark (DK)
- Karolinska Institutet (SE)
- Corresponding author
- Weischenfeldt, Joachim
- Grønbæk, Kirsten
- ORCID
- Venue
- Nature Communications
- Published
- 2021-10-18
- Volume
- 12
- Issue
- 1
- Pages
- 6061-6061
- ISSN
- 2041-1723 (ISSN-L)
- PMC
- PMC8523747
- OpenAlex
- W3205085619
- Cited by
- 108
- References
- 50
- Citations by year
- 2026: 19 · 2025: 19 · 2024: 17 · 2023: 30 · 2022: 23
- FWCI
- 12.25
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Nature Communications (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Research at the University of Copenhagen (University of Copenhagen) (publishedVersion, cc-by)
- University of Southern Denmark Research Portal (University of Southern Denmark) (submittedVersion, cc-by)
- RePEc: Research Papers in Economics (submittedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- Novo Nordisk Fonden (NNF17CC0027852)
- Topics
- Health Sciences › Medicine › Hematology › Acute Myeloid Leukemia Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Epigenetics and DNA Methylation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
- Keywords
- TET2 mutation, DNA hypermethylation, clonal hematopoiesis of indeterminate potential, clonal cytopenia of undetermined significance, acute myeloid leukemia, hematopoietic stem cells, myeloid differentiation, leukocyte function, immune response, transcription factor binding motifs, epigenetic regulators
- MeSH terms
- DNA Methyltransferase 3A, DNA (Cytosine-5-)-Methyltransferases, DNA-Binding Proteins, Enhancer Elements, Genetic, Hematopoiesis, Hematopoietic Stem Cells, Humans, Mutation, Myeloproliferative Disorders, Transcription Factors, DNA Methylation, Dioxygenases
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